Dartora Daniela Ravizzoni, Irigoyen Maria-Claudia, Casali Karina Rabello, Moraes-Silva Ivana C, Bertagnolli Mariane, Bader Michael, Santos Robson A S
a Cardiology Institute of Rio Grande do Sul/University Foundation of Cardiology, Porto Alegre, Rio Grande do Sul, Brazil.
b Heart Institute (InCor), University of São Paulo Medical School, São Paulo, São Paulo, Brazil.
Can J Physiol Pharmacol. 2017 Sep;95(9):993-998. doi: 10.1139/cjpp-2016-0557. Epub 2017 Apr 30.
Angiotensin-(1-7) counterbalances angiotensin II cardiovascular effects. However, it has yet to be determined how cardiovascular autonomic modulation may be affected by chronic and acute elevation of Ang-(1-7). Hemodynamics and cardiovascular autonomic profile were evaluated in male Sprague-Dawley (SD) rats and transgenic rats (TGR) overexpressing Ang-(1-7) [TGR(A1-7)3292]. Blood pressure (BP) was directly measured while cardiovascular autonomic modulation was evaluated by spectral analysis. TGR received A-779 or vehicle and SD rats received Ang-(1-7) or vehicle and were monitored for 5 h after i.v. administration. In another set of experiments with TGR, A-779 was infused for 7 days using osmotic mini pumps. Although at baseline no differences were observed, acute administration of A-779 in TGR produced a marked long-lasting increase in BP accompanied by increased BP variability (BPV) and sympathetic modulation to the vessels. Likewise, chronic administration of A-779 with osmotic mini pumps in TGR increased heart rate, sympathovagal balance, BPV, and sympathetic modulation to the vessels. Administration of Ang-(1-7) to SD rats increased heart rate variability values in 88% accompanied by 8% of vagal modulation increase and 18% of mean BP reduction. These results show that both acute and chronic alteration in the Ang-(1-7)-Mas receptor axis may lead to important changes in the autonomic control of circulation, impacting either sympathetic and (or) parasympathetic systems.
血管紧张素 -（1 - 7）可抵消血管紧张素II的心血管效应。然而，慢性和急性升高的血管紧张素 -（1 - 7）如何影响心血管自主神经调节尚待确定。在雄性Sprague - Dawley（SD）大鼠和过表达血管紧张素 -（1 - 7）的转基因大鼠 [TGR（A1 - 7）3292] 中评估了血流动力学和心血管自主神经特征。直接测量血压（BP），同时通过频谱分析评估心血管自主神经调节。TGR接受A - 779或赋形剂，SD大鼠接受血管紧张素 -（1 - 7）或赋形剂，并在静脉注射后监测5小时。在另一组针对TGR的实验中，使用渗透微型泵输注A - 779 7天。尽管在基线时未观察到差异，但在TGR中急性给予A - 779会导致血压显著持久升高，同时血压变异性（BPV）增加以及对血管的交感神经调节增加。同样，在TGR中用渗透微型泵慢性给予A - 779会增加心率、交感迷走神经平衡、BPV以及对血管的交感神经调节。给SD大鼠注射血管紧张素 -（1 - 7）可使88%的大鼠心率变异性值增加，同时迷走神经调节增加8%，平均血压降低18%。这些结果表明，血管紧张素 -（1 - 7）- Mas受体轴的急性和慢性改变均可能导致循环自主神经控制发生重要变化，影响交感神经和（或）副交感神经系统。
